CSF1R antagonism limits local restimulation of antiviral CD8+ T cells during viral encephalitis
Identifieur interne : 000D59 ( Main/Exploration ); précédent : 000D58; suivant : 000D60CSF1R antagonism limits local restimulation of antiviral CD8+ T cells during viral encephalitis
Auteurs : Kristen E. Funk [États-Unis] ; Robyn S. Klein [États-Unis]Source :
- Journal of Neuroinflammation [ 1742-2094 ] ; 2019.
Abstract
Microglia are resident macrophages of the central nervous system (CNS) locally maintained through colony-stimulating factor 1 receptor (CSF1R) signaling. Microglial depletion via CSF1R inactivation improves cognition in mouse models of neuroinflammation, but limits virologic control in the CNS of mouse models of neurotropic infections by unknown mechanisms. We hypothesize that CSF1R plays a critical role in myeloid cell responses that restrict viral replication and locally restimulate recruited antiviral T cells within the CNS.
The impact of CSF1R signaling during West Nile virus infection was assessed in vivo using a mouse model of neurotropic infection. Pharmacological inactivation of CSF1R was achieved using PLX5622 prior to infection with virulent or attenuated strains of West Nile virus (WNV), an emerging neuropathogen. The subsequent effect of CSF1R antagonism on virologic control was assessed by measuring mortality and viral titers in the CNS and peripheral organs. Immune responses were assessed by flow cytometric-based phenotypic analyses of both peripheral and CNS immune cells.
Mice treated with CSF1R antagonist prior to infection exhibited higher susceptibility to lethal WNV infection and lack of virologic control in both the CNS and periphery. CSFR1 antagonism reduced B7 co-stimulatory signals on peripheral and CNS antigen-presenting cells (APCs) by depleting CNS cellular sources, which limited local reactivation of CNS-infiltrating virus-specific T cells and reduced viral clearance.
Our results demonstrate the impact of CSF1R antagonism on APC activation in the CNS and periphery and the importance of microglia in orchestrating the CNS immune response following neurotropic viral infection. These data will be an important consideration when assessing the benefit of CSF1R antagonism, which has been investigated as a therapeutic for neurodegenerative conditions, in which neuroinflammation is a contributing factor.
The online version of this article (10.1186/s12974-019-1397-4) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s12974-019-1397-4
PubMed: 30704498
PubMed Central: 6354430
Affiliations:
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Funk</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2355 7002</institution-id><institution-id institution-id-type="GRID">grid.4367.6</institution-id><institution>Department of Internal Medicine, Division of Infectious Diseases,</institution><institution>Washington University School of Medicine,</institution></institution-wrap>Saint Louis, MO 63110 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Missouri (État)</region></placeName><wicri:cityArea>Saint Louis</wicri:cityArea></affiliation></author><author><name sortKey="Klein, Robyn S" sort="Klein, Robyn S" uniqKey="Klein R" first="Robyn S." last="Klein">Robyn S. Klein</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2355 7002</institution-id><institution-id institution-id-type="GRID">grid.4367.6</institution-id><institution>Department of Internal Medicine, Division of Infectious Diseases,</institution><institution>Washington University School of Medicine,</institution></institution-wrap>Saint Louis, MO 63110 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Missouri (État)</region></placeName><wicri:cityArea>Saint Louis</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2355 7002</institution-id><institution-id institution-id-type="GRID">grid.4367.6</institution-id><institution>Department of Pathology and Immunology,</institution><institution>Washington University School of Medicine,</institution></institution-wrap>Saint Louis, MO 63110 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Missouri (État)</region></placeName><wicri:cityArea>Saint Louis</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2355 7002</institution-id><institution-id institution-id-type="GRID">grid.4367.6</institution-id><institution>Department of Neurosciences,</institution><institution>Washington University School of Medicine,</institution></institution-wrap>Saint Louis, MO 63110 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Missouri (État)</region></placeName><wicri:cityArea>Saint Louis</wicri:cityArea></affiliation></author></analytic><series><title level="j">Journal of Neuroinflammation</title><idno type="eISSN">1742-2094</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p id="Par1">Microglia are resident macrophages of the central nervous system (CNS) locally maintained through colony-stimulating factor 1 receptor (CSF1R) signaling. Microglial depletion via CSF1R inactivation improves cognition in mouse models of neuroinflammation, but limits virologic control in the CNS of mouse models of neurotropic infections by unknown mechanisms. We hypothesize that CSF1R plays a critical role in myeloid cell responses that restrict viral replication and locally restimulate recruited antiviral T cells within the CNS.</p></sec><sec><title>Methods</title><p id="Par2">The impact of CSF1R signaling during West Nile virus infection was assessed in vivo using a mouse model of neurotropic infection. Pharmacological inactivation of CSF1R was achieved using PLX5622 prior to infection with virulent or attenuated strains of West Nile virus (WNV), an emerging neuropathogen. The subsequent effect of CSF1R antagonism on virologic control was assessed by measuring mortality and viral titers in the CNS and peripheral organs. Immune responses were assessed by flow cytometric-based phenotypic analyses of both peripheral and CNS immune cells.</p></sec><sec><title>Results</title><p id="Par3">Mice treated with CSF1R antagonist prior to infection exhibited higher susceptibility to lethal WNV infection and lack of virologic control in both the CNS and periphery. CSFR1 antagonism reduced B7 co-stimulatory signals on peripheral and CNS antigen-presenting cells (APCs) by depleting CNS cellular sources, which limited local reactivation of CNS-infiltrating virus-specific T cells and reduced viral clearance.</p></sec><sec><title>Conclusions</title><p id="Par4">Our results demonstrate the impact of CSF1R antagonism on APC activation in the CNS and periphery and the importance of microglia in orchestrating the CNS immune response following neurotropic viral infection. These data will be an important consideration when assessing the benefit of CSF1R antagonism, which has been investigated as a therapeutic for neurodegenerative conditions, in which neuroinflammation is a contributing factor.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (10.1186/s12974-019-1397-4) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Petersen, Lr" uniqKey="Petersen L">LR Petersen</name></author><author><name sortKey="Carson, Pj" uniqKey="Carson P">PJ Carson</name></author><author><name sortKey="Biggerstaff, Bj" uniqKey="Biggerstaff B">BJ Biggerstaff</name></author><author><name sortKey="Custer, B" uniqKey="Custer B">B Custer</name></author><author><name sortKey="Borchardt, Sm" uniqKey="Borchardt S">SM Borchardt</name></author><author><name sortKey="Busch, Mp" uniqKey="Busch M">MP 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Balmuth</name></author><author><name sortKey="Mitjans, M" uniqKey="Mitjans M">M Mitjans</name></author><author><name sortKey="Hertel, J" uniqKey="Hertel J">J Hertel</name></author><author><name sortKey="Habes, M" uniqKey="Habes M">M Habes</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chan, Ly" uniqKey="Chan L">LY Chan</name></author><author><name sortKey="Yim, Ekf" uniqKey="Yim E">EKF Yim</name></author><author><name sortKey="Choo, Abh" uniqKey="Choo A">ABH Choo</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Missouri (État)</li></region></list><tree><country name="États-Unis"><region name="Missouri (État)"><name sortKey="Funk, Kristen E" sort="Funk, Kristen E" uniqKey="Funk K" first="Kristen E." last="Funk">Kristen E. Funk</name></region><name sortKey="Klein, Robyn S" sort="Klein, Robyn S" uniqKey="Klein R" first="Robyn S." last="Klein">Robyn S. Klein</name><name sortKey="Klein, Robyn S" sort="Klein, Robyn S" uniqKey="Klein R" first="Robyn S." last="Klein">Robyn S. Klein</name><name sortKey="Klein, Robyn S" sort="Klein, Robyn S" uniqKey="Klein R" first="Robyn S." last="Klein">Robyn S. Klein</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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